Normal epithelial tissues have an intrinsic tumor suppression mechanism that eliminates oncogenic polarity-deficient cells from the tissue. We have previously found that clones of cells mutant for evolutionarily conserved apico-basal polarity genes, such as scribble or discs large, are eliminated from Drosophila epithelial tubular tissue though cell-cell communication. To dissect this tumor suppressive mechanism that eliminates polarity-deficient cells. we conducted a non-cell autonomous genetic screen in the eye imaginal disc. Wild-type cells surrounding polarity-deficient cells were mutagenized by EMS and mutations that modify the efficiency of cell competition were screened. We isolated a mutant eld-4 (elimination-defective-4), which fails to eliminate polarity-deficient cells from the tissue. Our genetic analysis revealed that eld-4 encodes a transmembrane protein that can act as a cell surface ligand. Furthermore, we identified its receptor expressing polarity-deficient cells. We are now analyzing the mechanism of cell elimination triggered by this ligand-receptor system. We are now also analyzing the physiological role of this ligand-receptor system.